Pain (78b, 81b, 82b) Flashcards
Actually all of this module could be called this
Which anesthetic does not interact with the GABA receptor?
Ketamine
What is the role of antidepressants in pain?
Treat neuorpathic pain by enhancing the descending inhibitory pathway
Which IV anesthetic is anti-emetic?
Propofol
Which pain medication is an NMDA antagonist?
Ketamine
During an operation, the patient’s aneurysm bursts
What should the anesthesiologist do?
Give a bolus of IV anesthetic to decrease cerebral blood flow so the bleed can be managed
Do not give inhaled bolus - these increase cerebral blood flow!
What is the role of nerve blocks in treating chronic pain?
- Diagnostic
- Figure out which nerve is the problem
- Prognostic
- Figure out if surgery will work
- Treatment
- Adjunctive
Which receptor is involved in “wind up”?
NMDA receptor (on the 2nd order neuron)
Results in a burst of nociceptive signals with C-fiber stimulation (even if many of the C-fiber signals are blocked by opioids)
What are the indications for ketamine during anesthesia?
High risk patinets with hemodynamic instability
Increases cerebral blood flow - do NOT use in patients with intracranial hypertension
Do NSAIDs or opioids have a role in neuropathic pain?
No
- Use antidepressants, anticonvulsants, or muscle relaxants instead
What is the MOA of barbituates for anesthesia?
What are they used for?
- Activates GABA-A receptor AND facilitates the binding of endogenous GABA to the GABA-A receptor
- Cl- conductance increases
- Hyperpolarization
- Used for induction of anesthesia
Normally, C-fibers go to lamina ___ of the dorsal horn, while A-beta fibers go to lamina ___
Normally, C-fibers go to lamina 2 of the dorsal horn, while A-beta fibers go to lamina 3
Effect on cerebral blood flow of…
- Most IV anesthetics:
- Volatile anesthetics:
- Most IV anesthetics: Decrease cerebral blood flow
- Except ketamine - increases flow and O2 demand
- Volatile anesthetics: Increase cerebral blood flow
- Due to vasodilation
Both decrease cerebral O2 demand (except ketamine)
The anterolateral tract transmits pain up the spinal cord, and then splits into 3 different pathways
- The _______ tract is for processing pain
- The _______ tract activated our emotional response to pain (fear)
- The _______ tract increases our awareness
- The neospinothalamic tract is for processing pain
- The paleospinothalamic tract activated our emotional response to pain (fear)
- The spinoreticular tract increases our awareness
What is the MOA of propofol for anesthesia?
- Activates the GABA-A receptor
Which method of central sensitization results in allodyina?
Neural sprouting
Which antiepileptic is most commonly used for neuropathic pain?
Gabapentin
Is the placebo effect a psychological phenomenon, or can it be explained by physiological changes in the body?
The placebo effect is NOT purely a psychological phenomenon
- There are endorhin-mediated phsyiologic changes that occur as a result of a placebo
- However, the placebo itself is not responsible for these changes
- Likely due to the brain’s reward system/what we expect from taking a medication??
What is the mechanism of action of ketamine?
NMDA receptor antagonist
- Works to treat pain even if wind up (central sensitization) has occurred
What is the mechanism of oral skeletal muscle relaxants?
Nonspecific supression of CNS polysynaptic pathways
Which drug would you give to counteract the hypotension (and reflex tachycardia) associated with propofol?
An alpha-1 agonist (ex: phenylephrine)
- Propopfol vasodilates
- Alpha-1 agnoists counteract by vasoconstricting
How do antiepileptic drugs work to treat chronic pain?
Block voltage-sensitive Na+ channels
- Decreases excitation and increases inhibition
- Fewer action potentials
- Increased threshold for repetitive action potential generation
- Prevents firing of burst neurons (wind up)
- Use for neuropathic pain!
What is the MOA of TCAs and SNRIs in treating pain?
- Block reuptake of 5HT and NE to enhance the descending inhibitory pathway
- Works to treat neuropathic pain
What is the MOA of etomidate?
In which patients would we use etomidate rather than propofol?
- Activates GABA-A receptors
- -> Increased Cl- conductance
- -> hyperpolarization
- More CV stability with etomidate than propofol, but causes nausea, vomiting, and adrenal cortical suppression
- Use in patients with ischemic heart disease who probably can’t tolerate propofol
How do opioids decrease pain?
- Decrease C-riber transmission
- Increase the activity of the descending inhibitory system
When is ketamine indicated for pain management?
- When opioids and NSAIDs are failing
- Other adjuncts have been tried
- Regional anesthesia (epidural, wound infiltration) is contraindicated
- The patient is in the hospital
- Given IV
What are the 3 major neurotransmitters of pain?
Glutamate
Substance P
CGRP
Which class of drugs promotes sedation, hypnosis, amnesia, and anxiolysis?
What is it used for?
Benzodiazapines
Used pre-op to reduce anxiety and promote amnesia
Note - NOT an analgesic; cannot activate the GABA receptor without endogenous GABA
What is the MOA of muscle relaxant drugs to treat chronic pain?
- GABA agonists potentiate the descending inhibitory system
- Cause sedation, centrally acting
- Tolerance in 2 weeks :(
- Alpha-2 agonists
- Tizanidine
- No tolerance :)
Don’t use soma!! (addictive tranquilizer)
